This application deals with a mechanism of leukemia resistance specified by the thymus of the F1 hybrids made by crossing "high leukemia" AKR strain with NZB mice. When the AKR strain, which produces high titers of ecotropic C-type RNA virus was crossed with the NZB strain, a high grade xenotropic virus producer, the progeny F1 mice expressed both viruses in high titers in all lymphoid tissues except their thymuses and thymus derived lymphocytes. Our goal is to analyze which subpopulation of cells in the F1 thymus is responsible for restricting the ecotropic retrovirus production and the mechanism of this restriction. Since this restriction was not found in the leukemia susceptible AKR thymus we shall attempt to identify by surface markers the subpopulation of thymocytes in AKR parents that specifically express the ecotropic virus. Since this thymus specific restriction is found only in the (AKR x NZB)F1 hybrid and not in F1 hybrids of AKR and other Fv-1n/n homozygous mice, the genetic mechanism of this restriction will be analyzed to elucidate if this is the manifestations of a NZB-derived T-lymphocyte defect. The specific cellular conditions necessary for the production of leukemogenic recombinant viruses will also be investigated since the leukemia resistant F1 hybrids failed to produce recombinant viruses in their peripheral lymphoid organs that expressed both ecotropic and xenotropic viruses in high titers.